A multistress responsive type I toxin-antitoxin system: bsrE/SR5 from the B. subtilis chromosome
A multistress responsive type I toxin-antitoxin system: bsrE/SR5 from the B. subtilis chromosome
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DOI：
10.1080/15476286.2016.1156288
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发表时间：
2016-03
期刊：
影响因子：
4.1
通讯作者：
P. Müller;N. Jahn;C. Ring;C. Maiwald;R. Neubert;C. Meißner;S. Brantl
中科院分区：
文献类型：
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作者：
P. Müller;N. Jahn;C. Ring;C. Maiwald;R. Neubert;C. Meißner;S. Brantl
bsrE/SR 5是来源于B类原噬菌体P6的I型TA系统。枯草染色体bsrE RNA编码30个氨基酸的毒素。抗毒素SR 5是一个163 nt的反义RNA。两个基因在其3′端重叠。bsrE的过表达导致琼脂平板上的细胞溶解，其可以被sr 5过表达中和，而染色体sr 5拷贝的缺失没有影响。SR 5是短暂的，半衰期为107分钟，而bsrE RNA是稳定的，半衰期>80分钟。sr 5启动子比bsrE启动子强10倍。SR 5与bsrE RNA的3′ UTR相互作用，从而通过募集RNase III促进其降解。RNase J1是负责SR 5和bsrE RNA降解的主要RNase，PnpA将SR 5前体加工成成熟RNA。Hfq稳定SR 5，但不是其抑制功能所必需的。bsrE RNA受温度冲击和碱胁迫的影响，而SR 5的量受各种胁迫的影响，其中包括pH、缺氧和铁限制。只有后者依赖于sigB。由于RNA酶Y的快速降解，这两种RNA在乙醇胁迫下极不稳定。
ABSTRACT bsrE/SR5 is a type I TA system from prophage-like element P6 of the B. subtilis chromosome. The 256 nt bsrE RNA encodes a 30 aa toxin. The antitoxin SR5 is a 163 nt antisense RNA. Both genes overlap at their 3′ ends. Overexpression of bsrE causes cell lysis on agar plates, which can be neutralized by sr5 overexpression, whereas deletion of the chromosomal sr5 copy has no effect. SR5 is short-lived with a half-life of ≈7 min, whereas bsrE RNA is stable with a half-life of >80 min. The sr5 promoter is 10-fold stronger than the bsrE promoter. SR5 interacts with the 3′ UTR of bsrE RNA, thereby promoting its degradation by recruiting RNase III. RNase J1 is the main RNase responsible for SR5 and bsrE RNA degradation, and PnpA processes an SR5 precursor to the mature RNA. Hfq stabilizes SR5, but is not required for its inhibitory function. While bsrE RNA is affected by temperature shock and alkaline stress, the amount of SR5 is significantly influenced by various stresses, among them pH, anoxia and iron limitation. Only the latter one is dependent on sigB. Both RNAs are extremely unstable upon ethanol stress due to rapid degradation by RNase Y.